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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Snoring (inspiratory noise related to narrowing of the upper airways) and obstructive sleep apnea (OSA) are two aspects of the same basic disorder: sleep-related narrowing of the upper airways. Patients with OSA have been heavy snorers for years and even decades. Lying supine induces snoring and mild OSA in heavy snorers due to hypotonia of pharyngeal dilator muscles, decreasing waking neural drive and recumbent position, which contribute to functional narrowing of the upper airways. Functional factors in obstruction during sleep include (a) respiratory instability prevalent in the male sex, (b) increased extensibility of the lax tissues surrounding the oro-pharynx and (c) deficient contraction of the pharyngeal dilator muscles during inspiration. These effects are worsened by sleep deprivation and fragmentation, alcohol intake and sedatives. Anatomical factors favoring narrowing of the upper airways in snorers and OSA patients are (a) abnormally narrow airways as well as (b) increased thickness and length of the velum palatinum in snorers and OSA patients, (c) tonsillar and adenoid hypertrophy, micro- and retrognathia, and nasal insufficiency, (d) obesity with fat infiltration of the soft tissues and in particular of the oropharynx, (e) relatively open mandibular angle, hypertrophy and thickness of the tongue, and lowered hyoid bone (as shown by MRI imaging). It is possible that many anatomical abnormalities may be the consequence of snoring and obstructive apnea. During NREM sleep the ineffective inspiratory efforts progressively increase with worsening hypoxia and hypercapnia. The upper airways become patent again when arousal induces phasic activation of the dilator pharyngeal muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenic aspects of snoring and obstructive apnea syndrome. 318 70

Changes in the longitudinal relaxation rate (R1) may play a role in the MRI signal intensity increases that have been associated with physiological brain activation. We used gradient-echo echo-planar MRI (GRE-EPI) to test whether physiological activations associated with hypercapnia in dogs were dependent on the delay (TR) between successive images in a time-series. Our results show that, in addition to activation-induced changes in the R2 (transverse relaxation including inhomogeneity effects), activation-induced changes in R1 are significant under certain pulsing conditions. In our paradigm, the R1 contribution became significant at TR values of 1 s or less.
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PMID:Blue blood or black blood: R1 effects in gradient-echo echo-planar functional neuroimaging. 779 46

Both arteriosclerosis and leukoaraiosis have a close relationship with hypertension, but the relationship between cerebral hemodynamics and leukoaraiosis in hypertensive patients has not been fully examined. To clarify this issue, we measured the regional cerebral blood flow (rCBF) and cerebrovascular response to hypercapnia in hypertensive patients with various degrees of leukoaraiosis. The subjects consisted of 7 normotensive normal controls and 17 hypertensive patients. The hypertensive patients were divided into three groups according to the severity of white matter lesions (leukoaraiosis) on MRI and the presence of dementia, namely, (1) negative or mild leukoaraiosis without dementia, (2) moderate to severe leukoaraiosis without dementia and (3) severe leukoaraiosis with dementia. Both the rCBF and the cerebrovascular response to hypercapnia were measured by the O-15 H2O bolus-injection method and positron emission tomography. The rCBF in hypertensive patients without dementia did not decrease when compared with the normotensive controls, but the rCBF in hypertensive patients with dementia markedly decreased in the cerebral cortices and white matter. On the other hand, the cerebrovascular response to hypercapnia declined with the severity of leukoaraiosis, and it decreased most severely in patients with severe leukoaraiosis and dementia. Our results indicate that the reduction in the cerebral hemodynamic reserve capacity has a close relationship with the severity of leukoaraiosis in hypertensive patients, although the rCBF is maintained in hypertensive patients without dementia, and suggest that arteriosclerotic change reduces cerebrovascular CO2 response and causes a leukoaraiosis in hypertensive patients.
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PMID:Cerebral blood flow and vascular response to hypercapnia in hypertensive patients with leukoaraiosis. 888 4

An issue in blood oxygenation level dependent contrast-based functional MRI is the accurate interpretation of the activation-induced signal changes. Hemodynamic factors other than activation-induced changes in blood oxygenation are known to contribute to the signal change magnitudes and dynamics, and therefore need to be accounted for or removed. In this paper, a general method for removal of effects other than activation-induced blood oxygenation changes from fMRI brain activation maps by the use of hypercapnic stress normalization is introduced. First, the effects of resting blood volume distribution across voxels on activation-induced BOLD-based fMRI signal changes are shown to be significant. Second, the effects of hypercapnia and hypoxia on resting and activation-induced signal changes are demonstrated. These results suggest that global hemodynamic stresses may be useful for non-invasive mapping of blood volume. Third, the normalization technique is demonstrated.
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PMID:A hypercapnia-based normalization method for improved spatial localization of human brain activation with fMRI. 943 Mar 48

We present an unusual case of weaning failure. A 67-yr-old man presented with confusion, hyponatremia, and hypercapnic respiratory failure that necessitated mechanical ventilation. CXR revealed a right hilar mass (non-small-cell carcinoma on biopsy). Level of consciousness improved with treatment of his hyponatremia. However, attempts at weaning were complicated by hypercapnia with no overt distress. Resistance and elastance were only slightly abnormal, excluding mechanics as a cause of respiratory failure. Maximal inspiratory pressure (MIP) and vital capacity (VC) were reduced at -15 cm H2O and 0.97 L, respectively. Limb muscle strength was well preserved, suggesting isolated respiratory muscle weakness. During a weaning trial respiratory rate increased from 7 to 40 breaths/min as PCO2 increased from 56 to 89 mm Hg, confirming an intact respiratory pacemaker and good response to CO2. However, spontaneous Pdi was only 1 to 2 cm H2O (< 20% of Pdimax) despite profound hypercapnia. The fact that the patient did not utilize a greater fraction of his pressure-generating capacity suggested preferential impairment of the automatic respiratory centers. MRI showed a large central metastatic lesion in the rostral medulla with only a thin rim of uninvolved tissue. This case illustrates the utility of relating the magnitude of spontaneous efforts to maximal voluntary efforts as a means of localizing the site of involvement in cases of respiratory muscle weakness. It also demonstrates that a large medullary mass lesion may selectively impair brainstem modulation of respiratory pressure output while sparing other medullary functions, and in particular the pacemaking function of the respiratory centers.
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PMID:Medullary metastasis causing impairment of respiratory pressure output with intact respiratory rhythm. 987 56

Ischemic lesions of the brainstem can lead to complex neurologic deficits. Failure of the automatic control of ventilation (Ondine's curse syndrome) is a possible but rare syndrome following localized brainstem dysfunction. We report on a 49-year-old man with intermittent bradycardia, cranial nerves' dysfunctions and a slight right-sided hemiparesis. An acute brainstem ischemia was diagnosed and treated immediately with high-dose heparin. Cerebral angiography revealed a proximal occlusion of the left vertebral artery but a normal right vertebral artery and a hyperplastic right posterior inferior cerebellar artery. Cranial Computed Tomography and MRI scan demonstrated multiple ischemic lesions in the posterior circulation. During a 4-week treatment course the patient underwent six episodes of acute severe hypoxia and hypercapnia requiring orotracheal intubation twice and manual ventilation by air mask over a few minutes for four times after a tracheostomy had been performed. Twice a short-term episode of hypothalamic Diabetes insipidus was observed following hypoventilation. We conclude that both Ondine's curse syndrome and diabetes insipidus were due to transient vertebrobasilar ischemia.
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PMID:Ondine's curse in association with diabetes insipidus following transient vertebrobasilar ischemia. 1053 7

The relationship between blood oxygenation level-dependent (BOLD) MRI signals, cerebral blood flow (CBF), and oxygen consumption (CMR(O2)) in the physiological steady state was investigated. A quantitative model, based on flow-dependent dilution of metabolically generated deoxyhemoglobin, was validated by measuring BOLD signals and relative CBF simultaneously in the primary visual cortex (V1) of human subjects (N = 12) during graded hypercapnia at different levels of visual stimulation. BOLD and CBF responses to specific conditions were averaged across subjects and plotted as points in the BOLD-CBF plane, tracing out lines of constant CMR(O2). The quantitative deoxyhemoglobin dilution model could be fit to these measured iso-CMR(O2) contours without significant (P </= 0.05) residual error and yielded MRI-based CMR(O2) measurements that were in agreement with PET results for equivalent stimuli. BOLD and CBF data acquired during graded visual stimulation were then substituted into the model with constant parameters varied over plausible ranges. Relative changes in CBF and CMR(O2) appeared to be coupled in an approximate ratio of approximately 2:1 for all realistic parameter settings. Magn Reson Med 42:849-863, 1999.
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PMID:Investigation of BOLD signal dependence on cerebral blood flow and oxygen consumption: the deoxyhemoglobin dilution model. 1054 43

Previous fMRI studies of the cerebrovascular response to hypercapnia have shown signal change in cerebral gray matter, but not in white matter. Therefore, the objective of the present study was to compare (15)O PET and T *(2)-weighted MRI during a hypercapnic challenge. The measurements were performed under similar conditions of hypercapnia, which were induced by inhalation of 5 or 7% CO(2). The baseline rCBF values were 65.1 ml hg(-1) min(-1) for temporal gray matter and 28.7 ml hg(-1) min(-1) for white matter. By linear regression, the increases in rCBF during hypercapnia were 23.0 and 7. 2 ml hg(-1) min(-1) kPa(-1) for gray and white matter. The signal changes were 6.9 and 1.9% for the FLASH sequence and were 3.8 and 1. 7% for the EPI sequence at comparable echo times. The regional differences in percentage signal change were significantly reduced when normalized by regional flow values. A deconvolution analysis is introduced to model the relation between fMRI signal and end-expiratory CO(2) level. Temporal parameters, such as mean transit time, were derived from this analysis and suggested a slower response in white matter than in gray matter regions. It was concluded that the differences in the magnitude of the fMRI response can largely be attributed to differences in flow and that there is a considerable difference in the time course of the response between gray and white matter.
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PMID:Regional differences in the CBF and BOLD responses to hypercapnia: a combined PET and fMRI study. 1067 82

Bold contrast MRI was applied for mapping vascular maturation in tumor- and wound-induced skin angiogenesis using the response of mature vessels to hypercapnia (inhalation of air vs. air 5% CO(2)) and the response of all vessels to hyperoxia (air 5% CO(2) vs. oxygen 5% CO(2) (carbogen)). MRI signal enhancement with hypercapnia was reduced in centered vs. linear phase encoding, suggesting increased blood flow. However, intravital microscopy demonstrated constriction of arterioles and reduced flux and density of red blood cells in mature capillaries with hypercapnia, with no change in the diameter of wound-induced neovasculature. The discrepancy in flow between MRI and intravital microscopy is consistent with increased plasma flow and reduced hematocrit. Hyperoxia resulted in increased blood oxygenation and constriction of all vessels. These results provide a hemodynamic explanation for the selective registration of MRI response to hypercapnia with mature vessels and the response to hyperoxia with total vascular function.
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PMID:In vivo BOLD contrast MRI mapping of subcutaneous vascular function and maturation: validation by intravital microscopy. 1132 16

Increases in cerebral blood flow produced by vasoactive agents will increase blood oxygen level-dependent (BOLD) MRI signal intensity. The effects of such vasodilation on activation-related signal changes are incompletely characterized. The two signal changes may be simply additive or there may be more a complex interaction. To investigate this, BOLD MRI was performed in four normal male subjects using T2*-weighted echo planar imaging; brain volumes were acquired every 6.2 s, using a Siemens VISION scanner operating at 2 Tesla; each volume consisted of 64 sequential transverse slices (64 x 64 pixels per slice, 3 x 3 x 3 mm). Sixteen periods of visual stimulation were produced using a flickering checkerboard (8 Hz, 31 s On/31 s Off); this was coupled with five periods of hypercapnia (4% inspired CO(2), 62 s On/124 s Off). Data were analyzed using SPM96. Mean signal intensity, calculated globally for the whole brain, closely mirrored changes in the partial pressure of end-tidal CO(2) (PCO(2)), and hypercapnia was associated with widespread significant signal increases (P < 0.001), predominantly within grey matter. As expected, the visual stimulation produced significant signal changes within the occipital cortex (P < 0.001). Within the occipital cortex, no significant interactions (P > 0.001) between the effects of the visual stimulation and PCO(2) were present. The increases in PCO(2) imposed dynamically in the present study would increase cerebral blood flow by between 25 and 40%, an increase within the physiological range and comparable to that induced by neural activation. With this flow change the effects of vasodilation, on an activation-related signal change, are simply additive.
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PMID:Does hypercapnia-induced cerebral vasodilation modulate the hemodynamic response to neural activation? 1135 26


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